Christian Scharenberg

ORCID: 0000-0003-2867-7809
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Acute Myeloid Leukemia Research
  • Chronic Lymphocytic Leukemia Research
  • Chronic Myeloid Leukemia Treatments
  • Hematopoietic Stem Cell Transplantation
  • Lymphoma Diagnosis and Treatment
  • Epigenetics and DNA Methylation
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Mast cells and histamine
  • Multiple Myeloma Research and Treatments
  • Hemoglobinopathies and Related Disorders
  • RNA Research and Splicing
  • Mesenchymal stem cell research
  • CAR-T cell therapy research
  • Genomic variations and chromosomal abnormalities
  • Platelet Disorders and Treatments
  • MicroRNA in disease regulation
  • Chemokine receptors and signaling
  • Immune cells in cancer
  • Neurogenesis and neuroplasticity mechanisms
  • Periodontal Regeneration and Treatments
  • Pluripotent Stem Cells Research
  • Porphyrin Metabolism and Disorders
  • Sarcoma Diagnosis and Treatment
  • Eosinophilic Disorders and Syndromes
  • Protein Degradation and Inhibitors

Skaraborg Hospital
2012-2024

Karolinska Institutet
2009-2019

Karolinska University Hospital
2009-2018

Center for Cancer Research
2010

Philipps University of Marburg
2007-2010

Georgetown University Medical Center
2010

Georgetown University
2010

National Institutes of Health
2010

National Cancer Institute
2010

International Society for Experimental Hematology
2009

Although the development of tyrosine kinase inhibitors (TKIs) to control unregulated activity BCR-ABL revolutionized therapy chronic myeloid leukemia, resistance TKIs is a clinical reality. Among postulated mechanisms overexpression ATP-binding cassette (ABC) transporters, such as P-glycoprotein (ABCB1) and breast cancer protein (ABCG2), which mediate reduced intracellular drug accumulation. We compared interactions imatinib, nilotinib, dasatinib with ABCB1 ABCG2 in ex vivo vitro systems....

10.1124/dmd.109.031302 article EN Drug Metabolism and Disposition 2010-04-27

A high proportion of patients with lower-risk del(5q) myelodysplastic syndromes will respond to treatment lenalidomide. The median duration transfusion-independence is 2 years some long-lasting responses, but almost 40% progress acute leukemia by 5 after starting treatment. mechanisms underlying disease progression other than the well-established finding small TP53-mutated subclones at diagnosis remain unclear. We studied a longitudinal cohort 35 low- and intermediate-1-risk treated...

10.3324/haematol.2016.152025 article EN cc-by-nc Haematologica 2016-11-24

Transplanted hematopoietic cells have previously been shown to contribute of other tissues by cell fusion. We wanted elucidate whether this phenomenon fusion also occurs under physiological conditions. Using a transgenic mouse reporter system irreversibly label the lineage, we were able test their contribution in absence any additional and potentially confounding factors such as irradiation or chemoablation. found genetically marked, fused Purkinje neurons well hepatocytes numbers comparable...

10.1523/jneurosci.5848-08.2009 article EN cc-by-nc-sa Journal of Neuroscience 2009-03-25

Summary The mechanisms underlying lenalidomide‐resistance of del(5q) MDS stem cells remain to be elucidated and may include cell‐intrinsic as well microenvironmental causes. Abnormal hypolobated megakaryocytes constitute one the hallmarks . We hypothesized that these have potential implications for regulation haematopoietic ( HSC ) similarly what has recently been described in murine system. Therefore, we conducted a study determine response abnormal lenalidomide therapy. studied...

10.1111/bjh.15094 article EN British Journal of Haematology 2018-01-29
Coming Soon ...